The main therapeutic hypertriglyceridemia medication are as follows

Hypertriglyceridemia medication are as follows:

Firstly, bile acid sequestrants (cholestyramine, colesevelam).

Bile acid sequestrants lower blood cholesterol levels by binding to bile acids in the intestine, causing more cholesterol to be converted to bile acids and excreted from the body. The dosage of cholestyramine is 16-24 grams per day, divided into 2 doses; and colesevelam 20-30 grams per day, divided into 2 doses.

hypertriglyceridemia medication
hypertriglyceridemia medication

Secondly, HMG-CoA reductase inhibitors (lovastatin, pravastatin, and simvastatin).

HMG-CoA reductase is the rate-limiting enzyme in cholesterol biosynthesis. If it is blocked, cells cannot synthesize cholesterol. After cholesterol synthesis is inhibited, the number of low-density lipoprotein (LDL) receptors on the surface of hepatocytes increases, leading to an increase in the amount of LDL absorbed by hepatocytes from the blood. The increase in LDL receptors results in an increase in the clearance of LDL-cholesterol, further reducing the level of LDL-cholesterol in the blood. The main action of HMG-CoA reductase inhibitors is to reduce cholesterol synthesis, increase LDL receptors, and lower LDL-cholesterol levels. These drugs reduce total cholesterol levels while also reducing triglyceride levels and increasing high-density lipoprotein (HDL) levels.

Thirdly, nicotinic acid and its derivatives (nicotinic acid, acipimox).

Very low-density lipoprotein (VLDL) is the precursor of LDL and the main carrier of triglycerides. Triglycerides are re-synthesized in the liver from free fatty acids released by adipose tissue. If there is a substance that can effectively block the release of fatty acids from adipose tissue, the liver cannot re-synthesize triglycerides.

When there is only a small amount of fatty acids, the liver synthesizes a small amount of triglycerides and a small amount of VLDL to transport triglycerides. This is the main mechanism of nicotinic acid and acipimox (Liponorm). It blocks the release of fatty acids from adipose tissue, reducing VLDL levels, because VLDL eventually converts to LDL, so reducing VLDL levels also reduces LDL levels.

Therefore, although this Hypertriglyceridemia medication mainly acts on the triglyceride synthesis process, it also reduces LDL levels, leading to a decrease in blood cholesterol levels. In addition, nicotinic acid and acipimox can increase HDL levels, which have a “protective” effect on the heart. The dosage of nicotinic acid is relatively large, 3-6 grams per day, so there are more adverse reactions.

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